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Using an unbiased approach, 16 cell lineages were assigned within 14,539 sequenced cells from patient\u2010matched SCD and non\u2010stricturing (NSCD) preparations. SCD and NSCD contained identical cell types. Amongst immune cells, B cells and plasma cells were selectively increased in SCD samples. B cell subsets suggested formation of tertiary lymphoid tissue in SCD and compared with NSCD there was an increase in IgG, and a decrease in IgA plasma cells, consistent with their potential role in CD fibrosis. Two Lumican\u2010positive fibroblast subtypes were identified and subclassified based on expression of selectively enriched genes as fibroblast clusters (C) 12 and C9. Cells within these clusters expressed the profibrotic genes\n                    <jats:italic>Decorin<\/jats:italic>\n                    (C12) and\n                    <jats:italic>JUN<\/jats:italic>\n                    (C9). C9 cells expressed\n                    <jats:italic>ACTA2<\/jats:italic>\n                    ; ECM genes\n                    <jats:italic>COL4A1<\/jats:italic>\n                    ,\n                    <jats:italic>COL4A2<\/jats:italic>\n                    ,\n                    <jats:italic>COL15A1<\/jats:italic>\n                    ,\n                    <jats:italic>COL6A3<\/jats:italic>\n                    ,\n                    <jats:italic>COL18A1<\/jats:italic>\n                    and\n                    <jats:italic>ADAMDEC1<\/jats:italic>\n                    ;\n                    <jats:italic>LAMB1<\/jats:italic>\n                    and\n                    <jats:italic>GREM1<\/jats:italic>\n                    . GO and KEGG Biological terms showed extracellular matrix and stricture organization associated with C12 and C9, and regulation of WNT pathway genes with C9. Trajectory and differential gene analysis of C12 and C9 identified four sub\u2010clusters. Intra sub\u2010cluster gene analysis detected 13 co\u2010regulated gene modules that aligned along predicted pseudotime trajectories.\n                    <jats:italic>CXCL14<\/jats:italic>\n                    and\n                    <jats:italic>ADAMDEC1<\/jats:italic>\n                    were key markers in module 1. Our findings support further investigation of fibroblast heterogeneity and interactions with local and circulating immune cells at earlier time points in fibrosis progression. Breaking these interactions by targeting one or other population may improve therapeutic management for SCD.\n                  <\/jats:p>","DOI":"10.1111\/jcmm.18344","type":"journal-article","created":{"date-parts":[[2024,4,30]],"date-time":"2024-04-30T01:06:45Z","timestamp":1714439205000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["Single cell sequencing data identify distinct B cell and fibroblast populations in stricturing Crohn's disease"],"prefix":"10.1111","volume":"28","author":[{"given":"David T.","family":"Humphreys","sequence":"first","affiliation":[{"name":"Victor Chang Cardiac Research Institute  Sydney New South Wales Australia"},{"name":"St Vincent's Clinical School University of New South Wales  Sydney New South Wales Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amy","family":"Lewis","sequence":"additional","affiliation":[{"name":"Centre for Genomics and Child 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